Abstract
Infants who are born prematurely are at significant risk of apnoea. In addition to the short-term consequences such as hypoxia, apnoea of prematurity has been associated with long-term morbidity, including poor neurodevelopmental outcomes. Clinical trials have illustrated the importance of methylxanthine drugs, in particular caffeine, in reducing the risk of long term adverse neurodevelopmental outcomes. However, the extent to which apnoea is causative of this secondary neurodevelopmental delay or is just associated in a background of other sequelae of prematurity remains unclear. In this review, we first discuss the pathophysiology of apnoea of prematurity, previous studies investigating the relationship between apnoea and neurodevelopmental delay, and treatment of apnoea with caffeine therapy. We propose a need for better methods of measuring apnoea, along with improved understanding of the neonatal brain's response to consequent hypoxia. Only then can we start to disentangle the effects of apnoea on neurodevelopment in preterm infants. Moreover, by better identifying those infants who are at risk of apnoea, and neurodevelopmental delay, we can work toward a risk stratification system for these infants that is clinically actionable, for example, with doses of caffeine tailored to the individual. Optimising treatment of apnoea for individual infants will improve neonatal care and long-term outcomes for this population.
Highlights
Apnoea of Prematurity (AOP) is frequently defined as a pause in breathing lasting more than 20 s, or more than 10 s with accompanying bradycardia and/ or oxygen desaturations in an infant born before 37 weeks’ gestation [1,2,3]
Can we predict which infants are most at risk of experiencing apnoea and when? Which of these will be improved with dose-stratified caffeine treatment? Which infants with AOP are most at risk of long-term neurodevelopmental deficits? To address these questions, we propose that we first need [1] improvements in AOP measurement in the Neonatal Intensive Care Unit (NICU) and [2] a better understanding of the impact of apnoea on brain development in preterm infants
To our knowledge, the only investigation to consider the relationship with AOP so far is the volumetric MRI studies of 70 Caffeine for Apnoea of Prematurity (CAP) trial cohort patients, which found no substantial differences in gross brain volume or white matter distribution, except for a small decrease in growth of the corpus callosum in the caffeine treated group compared with the placebo controls [111]
Summary
Apnoea of Prematurity (AOP) is frequently defined as a pause in breathing lasting more than 20 s, or more than 10 s with accompanying bradycardia and/ or oxygen desaturations in an infant born before 37 weeks’ gestation [1,2,3]. Along with acute morbidities such as cyanosis and chronic intermittent hypoxia, a key consideration for these infants is whether AOP influences their health later in life. This is the case with regards to the central nervous system, which is highly sensitive to hypoxia. We will review the existing literature with regards to the mechanisms of AOP and its possible role in long-term neurodevelopmental disorders in premature infants. We discuss key research questions in this area moving forward and approaches to investigate these problems
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
